Respiratory Flashcards
4 most common drugs against TB
(Isoniazid) INH: primary drug used
rifampin
ethambutol
pyrazinamide
Isoniazid MOA
Suppresses bacterial growth by inhibiting synthesis of mycolic acid, a component of the mycobacterial cell wall.
Metabolized in the liver through acetylation—watch for “slow acetylators”
Isoniazid A/E and what to administer in high risk pt groups
Hepatotoxicity
Peripheral neuropathy
- Administer pyridoxine (Vitamin B6) daily in high risk groups (i.e., DM, ETOH abuse) or if patient develops neuropathy
Rifampin MOA
MOA: inhibits bacterial DNA-dependent RNA polymerase -> results in suppression of RN synthesis and protein synthesis
A/E of Rifampin
discoloration of bodily fluids
2 Analogs of Rifampin (close chemical make-up with same MOA and A/E)
Rifapentine
Rifabutin
Pyrazinamide (PZA) A/E
Non-gouty polyarthralgias – (pain in multiple joints)
Ethanbutol A/E
Optic neuritis – blurred vision, constriction of visual fields, & disturbance of color discrimination (red-green color blindness).
What is the most effective drug class for prevention / treatment of seasonal & perennial rhinitis - it reduces inflammation and edema
Intranasal Glucocorticoids (-sone)
Difference between H1 and H2 blockers (antihistamine)
H1 blockers are the drugs to which most people are referring when they use the term antihistamine. H1 blockers prevent the harmful effects of histamine and are used to treat seasonal allergic rhinitis, anaphylaxis, reactions to insect bites, and so forth.
H2 blockers are used to treat gastric acid disorders
When to take first generation antihistamines?
take at bedtime to avoid sedation
How to recognize first generation anti-histamine?
-amine
Common second generation anti-histamines?
Zyrtec, Claritin, Clarinex, Allegra
What is major difference between first and second generation anti-histamines?
Second generation poorly cross the blood-brain barrier; have a low affinity for H1 receptors in the CNS therefore does not cause sedation
Sympathomimetics (Decongestants) MOA
Reduce nasal congestion via activation of alpha1 adrenergic receptors on nasal blood vessels -> vasoconstriction